This document discusses several types of cardiac dysrhythmias including sinus tachycardia, sinus bradycardia, premature atrial contractions, paroxysmal atrial tachycardia, atrial flutter, and atrial fibrillation. For each dysrhythmia, the document discusses etiology, characteristics based on ECG analysis, and general management approaches.

1. Cardiac Dysrhythmias
S Makonde

3. • Cardiac dysrhythmias are disturbances in regular heart
rate and/ or rhythm due to change in electrical
conduction or automaticity.
• Dysrhythmias may arise from the sinoatrial (SA) node
(sinus bradycardia or tachycardia) or anywhere within
the atria or ventricles (known as ectopy or ectopic
beats). Some may be benign and asymptomatic,
whereas other dysrhythmias are life-threatening.
• Dysrhythmias may be detected by change in pulse,
abnormality on auscultation of heart rate, or ECG
abnormality. Continuous cardiac monitoring is
indicated for potentially life-threatening dysrhythmias.

4. Sinus Tachycardia
Aetiology
• Sympathetic nerve fibres, which act to speed up
excitation of the SA node, are stimulated by
underlying causes, such as anxiety, exercise, fever,
shock, drugs, altered metabolic states (such as
hyperthyroidism), or electrolyte disturbances.
• The wave of impulse is transmitted through the
normal conduction pathways; the rate of sinus
stimulation is simply greater than normal (rate
exceeds 100 beats/minute).

5. Analysis
• Rate: 100 to 150 beats/minute.
• Rhythm: R-R intervals are regular.
• P wave: present for each QRS complex, normal configuration, and
each P wave is identical or may be buried in previous T wave.
• PR interval: falls between 0.12 and 0.20, or 0.16 second.
• P wave may be hidden in preceding T wave in rapid rates.
• QRS complex: normal in appearance, one follows each P wave.
• QRS interval: <0.11 seconds.
• T wave: follows each QRS complex and is positively conducted.
• QT interval: <0.48 seconds.

7. Management
• Treatment is directed toward elimination of
the cause rather than the dysrhythmia.
• Urgency is dependent on the effect of rapid
heart rate on coronary artery filling time to
prevent cardiac ischemia.
• Administration of oxygen and normal saline
solution should be considered as initial
treatment.

8. Sinus Bradycardia
Etiology
• The parasympathetic fibres (vagal tone) are stimulated and cause
the sinus node to slow.
• Underlying causes:
– a. Drugs.
– b. Altered metabolic states such as hypothyroidism.
– c. The process of aging, which causes increasing fibrotic tissue and
scarring of the SA node.
– d. Certain cardiac diseases such as acute MI (especially inferior wall
MI).
• The wave of impulse is transmitted through the normal conduction
pathways; the rate of sinus stimulation is simply less than normal
(less than 60 beats/minute).

9. Analysis
• Rate: <60 beats/minute.
• Rhythm: R-R interval is regular.
• P wave: present for each QRS complex, normal
configuration, and each P wave is identical.
• PR interval: falls between 0.12 and 0.18 second.
• QRS complex: normal in appearance, one follows each
P wave.
• QRS interval: 0.04 to 0.11 second.
• T wave: follows each QRS and is positively conducted.

11. Management
• The urgency of treatment depends on the effect
of the slow rate on maintenance of CO.
• Atropine 0.5 mg IV push blocks vagal stimulation
to the SA node and therefore accelerates heart
rate. Dopamine or epinephrine are alternatives if
atropine is ineffective.
• If bradycardia persists, a pacemaker may be
required.
• Sinus bradycardia is common in athletic
individuals and does not require treatment.

12. Premature Atrial Contraction
Aetiology
• May occur in the healthy heart where they are
idiopathic and benign.
• In the diseased heart, premature atrial
contractions (PACs) may represent ischemia and a
resultant irritability in the atria. They may
increase in frequency and be the precursor of
more serious dysrhythmias.
• May be caused by electrolyte abnormalities,
hypoxia, MI, heart failure, and acid-base
disturbances.

13. • The wave of impulse of the PAC originates within
the atria and outside the sinus node. Because the
impulse originates within the atria, the P wave
will be present, but it will be different in
appearance as compared with those beats
originating within the sinus node.
• The impulse traverses the remainder of the
conduction system in a normal pattern; thus, the
QRS complex is identical in configuration to the
normal sinus beats.

14. Analysis
• Rate: may be slow or fast.
• Rhythm: will be irregular, caused by the early occurrence of thePAC.
• P wave: will be present for each normal QRS complex; the P wave of
the premature contraction will be distorted in shape.
• PR interval: may be normal but can also be shortened, depending
on where in the atria the impulse originated. (The closer the site of
atrial impulse formation to the atrioventricular [AV] node, the
shorter the PR interval will be.)
• QRS complex: within normal limits because all conduction below
the atria is normal.
• T wave: normally conducted.

16. Management
• Generally requires no treatment if laboratory
values are normal.
• PACs should be monitored for increasing
frequency.

17. Paroxysmal Atrial Tachycardia
Aetiology
• Causes include:
– Syndromes of accelerated pathways (eg, Wolff-
Parkinson- White syndrome).
– Syndrome of mitral valve prolapse.
– Ischemic CAD.
– Excessive use of alcohol, cigarettes, caffeine.
– Drugs—digoxin is a frequent cause.

18. • An ectopic atrial focus captures the rhythm of
the heart and is stimulated at a very rapid
rate; the impulse is conducted normally
through the conduction system so the QRS
complex usually appears within normal limits.
• The rate is often so rapid that P waves are not
obvious but may be “buried” in the preceding
T wave.

19. Analysis
• Rate: between 150 and 250 beats/minute.
• Rhythm: regular.
• P wave: present before each QRS complex; however,
the faster the rate, the more difficult it becomes to
visualize P waves. (The P waves can frequently be
measured with calipers by observing the varying
configuration of the preceding T waves.)
• PR interval: usually not measurable.
• QRS complex: will appear normal in configuration and
within 0.06 to 0.10 second.
• T wave: will be distorted in appearance as a result of P
waves being buried in them.

21. Management
• Treatment is directed first to slowing the rate
and, second, to reverting the dysrhythmia to a
normal sinus rhythm.
• Reducing the rate may be accomplished by having
the patient perform a Valsalva maneuver. This
stimulates the vagus nerve to slow the heart.
– a. A Valsalva maneuver may be done by having the
patient gag or “bear down” as though attempting to
have a bowel movement.
– b. The health care provider may choose to perform
carotid massage.

22. • Adenosine is the drug of choice for paroxysmal
atrial tachycardia associated with hypotension,
chest pain, or shortness of breath.
– a. The initial dose is 6 mg rapid IV push followed by a
fast normal saline flush. If there is no response in 1 to
2 minutes, a second and third bolus of 12 mg may be
given, each followed by fast normal saline flushes.
– b. Has a very short half-life and is therefore eliminated
quickly.

23. • IV beta-adrenergic blockers, such as esmolol,
may be used.
• Calcium channel blockers (eg, verapamil) are
effective in reverting this dysrhythmia. Beware
of hypotension, however, especially in the
volume-depleted patient.
• If drug therapy is ineffective, elective
cardioversion can be used.

24. Atrial Flutter
Aetiology
• Occurs with atrial stretching or enlargement (as
in AV valvular disease), MI, and heart failure.
• An ectopic atrial focus captures the rhythm in
atrial flutter and fires at an extremely rapid rate
(200 to 400 beats/minute) with regularity.
• Conduction of the impulse through the
conduction system is normal; thus, the QRS
complex is unaffected.

25. • An important feature of this dysrhythmia is that
the AV node sets up a therapeutic block, which
disallows some impulse transmission.
– a. This can produce a varying block or a fixed block (ie,
sometimes the AV node will transmit every second
flutter wave, producing a 2:1 block, or the rhythm can
be 3:1 or 4:1).
– b. If the AV node conducted 1:1, then the outcome
would be a ventricular rate of about 300
beats/minute. The patient would rapidly deteriorate.

26. Analysis
• Rate: atrial rate between 250 and 400 beats/minute;
ventricular rate will depend on degree of block.
• Rhythm: regular or irregular, depending on kind of block .
• P wave: not present; instead, it is replaced by a saw-
toothed pattern that is produced by the rapid. firing of the
atrial focus.
• These waves are also referred to as “F” waves.
• PR interval: not measurable.
• QRS complex: normal configuration and normal conduction
time.
• T wave: present but may be obscured by flutter waves.

27. Management
• The urgency of treatment depends on the
ventricular response rate and resultant
symptoms. Too rapid or slow a rate will decrease
CO.
• A calcium channel blocker, such as diltiazem, may
be used to slow AV nodal conduction. Use with
caution in the patient with heart failure,
hypotension, or concomitant beta adrenergic
blocker therapy.
• Digoxin may be used.

28. • An IV beta-adrenergic blocker, such as
esmolol, may also be used.
• If drug therapy is unsuccessful, atrial flutter
will typically respond to cardioversion.
• Small doses of biphasic electrical current (50
to 100 joules) are usually successful.
• Electrophysiologic studies and subsequent
ablation therapy are highly effective because
the ectopic focus is usually readily identified.

30. Atrial Fibrillation
Aetiology
• Fibrotic changes associated with the aging
process, acute MI, valvular diseases, and digoxin
preparations may cause atrial fibrillation.
• Fluid shifts in body (ie, after hemodialysis or
surgery).
• Multiple atrial foci fire impulses at rapid and
disorganized rates.
• The atria are not depolarized effectively; thus,
there are no well-formed P waves.

31. • Instead, the baseline between QRS complexes is filled
with a “wiggly” line that is described as fine or coarse.
• If the atrial rate is rapid enough, the line will appear
almost flat. The atria are said to be firing at rates of
between 300 and 500 times per minute.
• The conduction of a QRS complex is so random that the
rhythm is extremely irregular.
• Atrial fibrillation may be described as controlled if the
ventricular response is 100 beats/minute or less; the
dysrhythmia is uncontrolled if the rate is above 100
beats/minute.

32. • Analysis
• Rate: atrial fibrillation is usually immeasurable because fibrillatory
• waves replace P waves; ventricular rate may vary from bradycardia
• to tachycardia.
• Rhythm: classically described as an “irregular irregularity.”
• P wave: replaced by fibrillatory waves, sometimes called “little f ”
• waves.
• PR interval: not measurable.
• QRS complex: a normally conducted complex.
• T wave: normally conducted.

33. Management
• Controlled atrial fibrillation of long-standing duration
requires no treatment as long as the patient is
experiencing no untoward effects. Most cardiologists
agree that reversion of long-standing atrial fibrillation
is hazardous because of the potential for a thrombus to
be dislodged from the atria at the time of reversion.
• Uncontrolled atrial fibrillation (ventricular responses of
100 beats/minute or greater) is treated with beta-
adrenergic blocker or calcium channel blockers to
control rate at rest and activity. If the atrial fibrillation
is of recent onset, the cardiologist may choose to
revert the rhythm to a sinus rhythm.

34. • Digoxin is a second-line drug for rate control
because it only controls rate at rest.
• Cardioversion (electrical or pharmacologic) for
recent-onset atrial fibrillation may be required
starting with low amounts of biphasic
electrical current (100 to 200 joules).
• Chronic anticoagulation therapy may be
warranted to prevent microemboli.

36. Premature Ventricular Contraction
Aetiology
• May be caused by acute MI, other forms of heart disease,
pulmonary diseases, electrolyte disturbances, metabolic
instability, and drug abuse.
• The wave of impulse originates from an ectopic focus (foci)
within the ventricles at a rate faster than the next normally
occurring beat.
• Because the normal conduction pathway is bypassed, the
configuration of the premature ventricular contraction
(PVC) is wider than normal and is distorted in appearance.
PVCs may occur in regular sequence with normal rhythm—
every other beat (bigeminy), every third beat (trigeminy),
and so forth

37. • Analysis
• Rate: may be slow or fast.
• Rhythm: will be irregular because of the premature firing of the
ventricular ectopic focus.
• P wave: will be absent because the impulse originates in the
ventricle, bypassing the atria and AV node.
• PR interval: not measurable.
• QRS complex: will be widened greater than 0.12 second, bizarre in
appearance when compared with normal QRS complex.
• (The QRS of a PVC is commonly referred to as having a “sore
thumb” appearance.)
• T wave: the T wave of the PVC is usually deflected opposite to the
QRS.

39. Management
• Management
• PVCs are usually the precursors of more serious
ventricular dysrhythmias. The following conditions
involving PVCs require prompt and vigorous treatment,
especially if the patient is symptomatic or unstable:
– a. PVCs occurring at a rate exceeding six per minute.
– b. Occur as two or more consecutively.
– c. PVCs fall on the peak or down slope of the T wave
(period of vulnerability).
– d. Are of varying configurations, indicating a multiplicity of
foci.

40. • Historically, the standard treatment for PVCs has been
lidocaine. Today, however, amiodarone IV is the
preferred method due to lidocaine’s risk for toxicity.
– a. Can be given by bolus of 150 mg IV over 10 minutes.
– b. IV infusion consists of a loading dose of 1 mg/minute for
6 hours, followed by a maintenance rate of 0.5 mg/minute
for 18 hours.
– c. After IV load, patient may require oral dosing.
• Lidocaine toxicities include confusion and slurred
speech. It should be used with caution in older adults
and in those with liver disease.

41. Ventricular Tachycardia
Aetiology
• Occurs with:
– a. Acute MI, cardiomyopathy.
– b. Syndromes of accelerated rhythm that deteriorate (eg, Wolff-
Parkinson-White syndrome).
– c. Metabolic acidosis, especially lactic acidosis.
– d. Electrolyte disturbance.
– e. Toxicity to certain drugs, such as digoxin or isoproterenol.
• A life-threatening dysrhythmia that originates from an
irritable focus within the ventricle at a rapid rate. Because
the ventricles are capable of an inherent rate of 40
beats/minute or less, a ventricular rhythm at a rate of 100
beats/minute may be considered tachycardia.

42. • Analysis
• Rate: usually between 100 and 220 beats/minute.
• Rhythm: usually regular but may be irregular.
• P wave: not present.
• PR interval: not measurable.
• QRS complex: broad, bizarre in configuration,
widened greater than 0.12 second.
• T wave: usually deflected opposite to the QRS
complex.

44. Management
• Ventricular tachycardia (VT) less than 30 seconds is called
nonsustained VT. VT more than 30 seconds is sustained VT
and requires immediate treatment.
• If the patient has a pulse and is hemodynamically stable,
medications are the initial treatments. Amiodarone IV
bolus can be given to halt the dysrhythmia. Other potential
medications that may be used (if amiodarone fails) include
lidocaine and procainamide. If patient becomes
hemodynamically unstable, prepare for synchronized
cardioversion with 200 joules of biphasic electrical current.
• If the patient is pulseless, defibrillation is recommended
with 200 joules of biphasic electrical current.

45. • The purpose of cardioversion/defibrillation is to
abolish all abnormal electrical activity and allow
the intrinsic cardiac rhythm the opportunity to
restart.
• In some cases, VT may be refractory to drug
therapy. Nonpharmacologic treatments, such as
endocardial resection, aneurysmectomy,
antitachycardia pacemakers, cryoablation,
automatic internal defibrillators, and catheter
ablation, are alternative treatment modalities.

46. • An atypical form of VT, referred to as polymorphous VT or torsades
de pointes (twisting of the points), can result as a consequence of
drug therapy (eg, quinidine therapy) or electrolyte imbalance such
as hypomagnesemia. It is important to diagnose polymorphous VT
as the treatment differs from monomorphic VT.
– a. Torsades de pointes is characterized by a QT interval prolonged to
greater than 0.60 second, varying R-R intervals, and polymorphous
QRS complexes.
– b. The treatment of choice is administration of magnesium sulfate 1 g
IV over 5 to 60 minutes.
– c. If the patient loses consciousness and pulse, defibrillate with 120 to
200 joules of biphasic electrical current.
– d. Ventricular pacing to override the ventricular rate and, thus, capture
the rhythm is also an acceptable treatment.
– e. Procainamide should be avoided because its effect is to prolong the
QT interval.

47. Ventricular Fibrillation
Aetiology
• Occurs in acute MI, acidosis, electrolyte
disturbances, and other deteriorating ventricular
rhythms.
• The ventricles are firing chaotically at rates that
exceed 300 beats/minute, resulting in ineffective
impulse conduction.
• CO ceases, and the patient loses pulse, BP, and
consciousness.
• Must be reversed immediately or the patient will
die.

48. Analysis
• Rate: not measurable because of absence of
well-formed QRS complexes.
• Rhythm: chaotic.
• P wave: not present.
• QRS complex: bizarre, chaotic, no definite
contour.
• T wave: not apparent.

50. Management
• The only treatment for ventricular fibrillation is
immediate defibrillation.
• Defibrillate at 120 to 200 joules with a biphasic
defibrillator.
• Current advanced cardiac life support guidelines no
longer recommend three stacked shocks before
initiating CPR and medication administration.
• Epinephrine or vasopressin are first-line drugs after
defibrillation because these drugs may make the
fibrillation more vulnerable to defibrillation.

51. • Unsuccessful defibrillation may be a result of
lactic acidosis (treatable with sodium
bicarbonate).
• Check adequacy of the high-quality CPR being
performed:
– 100 compressions/minute at a 2 to 2.-inch depth.

52. Atrioventricular Block
Etiology
• May be caused by ischemia or inferior wall MI,
digoxin toxicity, hypothyroidism, or Stokes-Adams
syndrome.
• Impaired tissue at the level of the AV node
prevents the timely passage of the wave of
impulse through the conduction system.
• In first-degree AV block, the impulse is
transmitted normally, but it is delayed at the level
of the AV node. The PR interval exceeds 0.20
second.

53. • In second-degree AV block, two or more atrial impulses
occur before the ventricles are stimulated.
– a. Second-degree type 1 (Mobitz 1 Wenckebach)—block occurs
above the AV node. There is an increase in delay of electrical
impulse (increasing PR interval) with every beat until one P
wave fails to conduct and is not followed by a QRS complex
(beat is dropped). Mobitz type 1 is usually a temporary and
benign dysrhythmia and seldom requires intervention (pacing)
unless ventricular rate is slow and the patient is unstable.
– b. Second-degree type 2 (Mobitz 2)—block occurs below the AV
node in the bundle of His or bundle-branch system.
– The atria and ventricles are discharging impulses but the activity
bears no relationship to each other. There is a sudden failure to
conduct an atrial impulse to the ventricles without a delay of
the PR interval.

54. • In third-degree AV block, or complete heart
block, the electrical impulse is completely
blocked from the SA node to the AV node. An
independent pacemaker in the ventricles
takes over at a much slower rate than the atria
and are firing independently of each other.

55. • Analysis
• 1. First-degree AV block .
• Rate: usually normal but may be slow.
• Rhythm: regular.
• P wave: present for each QRS complex, identical in
configuration.
• PR interval: prolonged to greater than 0.20 second.
• QRS complex: normal in appearance and between 0.06
and 0.10 second.
• T wave: normally conducted.

56. • Second-degree AV block
• Rate: usually normal.
• Rhythm: may be regular or irregular.
• P wave: present but some may not be followed by a
QRS complex. A ratio of two, three, or four P waves to
one
• QRS complex may exist.
• PR interval: varies in Mobitz I (Wenckebach), usually
lengthens,until one is not conducted; constant in
Mobitz II, but not all P waves conducted.
• T wave: normally conducted.

57. • Third-degree AV block (complete heart block).
• Rate: atrial rate is measured independently of the
ventricular rate; the ventricular rate is usually very slow.
• Rhythm: each independent rhythm will be regular, but they
will bear no relationship to each other.
• P wave: present but no consistent relationship with the
QRS.
• PR interval: not really measurable.
• QRS complex: depends on the escape mechanism (ie, AV
node will have normal QRS, ventricular will be wide and the
rate will be slower).
• T wave: normally conducted.

58. Management
• Like that of other dysrhythmias, the treatment
of heart blocks depends on the effect the rate
is having on CO.
• First-degree AV block usually requires no
treatment.
• Second-degree AV block, type 1 and type 2,
may require treatment if the ventricular rate
falls too low to maintain effective CO. Mobitz
type 2 is more serious than Mobitz type 1.

59. • Third-degree AV block usually requires intervention.
However, some patients may be able to tolerate third-
degree block for a length of time.
• Transcutaneous pacing should be employed in the
emergent situation while transvenous pacing is being
set up.
• Atropine may be given while awaiting the pacemaker,
but it must be remembered that the effect of atropine
is to block vagal tone, and the vagus acts on the sinus
node. Because the AV node is the culprit in heart block,
atropine may not be helpful.